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L-NG-硝基精氨酸（L-NOARG），一种新型的、体外可逆转内皮依赖性血管舒张的L-精氨酸抑制剂。

L-NG-nitro arginine (L-NOARG), a novel, L-arginine-reversible inhibitor of endothelium-dependent vasodilatation in vitro.

作者信息

Moore P K, al-Swayeh O A, Chong N W, Evans R A, Gibson A

机构信息

Biomedical Sciences Division, King's College London.

出版信息

Br J Pharmacol. 1990 Feb;99(2):408-12. doi: 10.1111/j.1476-5381.1990.tb14717.x.

DOI:10.1111/j.1476-5381.1990.tb14717.x
PMID:2328404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1917379/
Abstract
  1. The effect of L-NG-nitro arginine (L-NOARG) was compared with that of L-NG-monomethyl arginine (L-NMMA) on vasodilatation of the isolated aorta of the rabbit and perfused mesentery of the rat in response to acetylcholine (ACh) and sodium nitroprusside (NP). 2. L-NOARG (1.5-100 microM) and L-NMMA (3-100 microM) produced concentration-related contraction of the rabbit aorta precontracted with phenylephrine (700-900 nM). Similarly, L-NOARG (10-200 microM) and L-NMMA (30-100 microM) elevated perfusion pressure of the noradrenaline (NA, 0.6-2.5 mM)-preconstricted rat mesentery preparation. 3. L-NOARG (1.5-100 microM) and L-NMMA (3-100 microM) caused concentration-related inhibition of the vasodilator effect of ACh (0.01-1.0 microM) on the rabbit aorta without influencing responses to NP (0.03-0.5 microM). L-NOARG methyl ester (30 microM) also inhibited ACh-induced vasorelaxation with similar potency to NOARG. L-arginine (30-150 microM) but not D-arginine (100 microM) caused graded reversal of the inhibitory effect of both L-NOARG (15 microM) and L-NMMA (30 microM). Complete reversal of the effect of both inhibitors was achieved with 150 microM L-arginine. L-Alanine (50 microM), L-arginosuccinic acid (5 microM), L-citrulline (50 microM), L-methionine (50 microM) and L-ornithine (50 microM) failed to reverse the inhibitory effect of L-NOARG (15 microM). 4. L-NOARG (10-200 microM) and L-NMMA (30-100 microM) inhibited the vasodilator effect of ACh (0.006-18.0 nmol) in the rat mesentery without affecting vasodilatation due to NP (1.1-11.1 nmol). L-Arginine (100 microM) but not D-arginine (100 microM) produced partial reversal of the effect of L-NOARG (30 microM) and L-NMMA (30 microM). 5. L- and D-N'-butyloxycarbonyl No-nitro arginine (100 microM) produced modest (approximately 20%) inhibition of the effect of ACh on the rabbit aorta; this effect was not reversible with L-arginine (100 microM). L-Namonocarbobenzoxy arginine (L-NMCA, 5O microM), L-N-NG-dicarbobenzoxy arginine (L-NDCA, 5 microM) and L-NG-tosyl arginine (50 microM) were inactive. 6. These results identify L-NOARG as a potent, L-arginine reversible inhibitor of endothelium-dependent vasodilatation. The available data suggests that L-NOARG, like L-NMMA, inhibits endothelial nitric oxide (NO) biosynthesis.
摘要
  1. 将L-NG-硝基精氨酸（L-NOARG）与L-NG-单甲基精氨酸（L-NMMA）对兔离体主动脉和大鼠灌注肠系膜对乙酰胆碱（ACh）和硝普钠（NP）反应的血管舒张作用进行了比较。2. L-NOARG（1.5 - 100微摩尔）和L-NMMA（3 - 100微摩尔）使预先用去氧肾上腺素（700 - 900纳摩尔）预收缩的兔主动脉产生浓度依赖性收缩。同样，L-NOARG（10 - 200微摩尔）和L-NMMA（30 - 100微摩尔）使去甲肾上腺素（NA，0.6 - 2.5毫摩尔）预收缩的大鼠肠系膜制备物的灌注压力升高。3. L-NOARG（1.5 - 100微摩尔）和L-NMMA（3 - 100微摩尔）对ACh（0.01 - 1.0微摩尔）对兔主动脉的血管舒张作用产生浓度依赖性抑制，而不影响对NP（0.03 - 0.5微摩尔）的反应。L-NOARG甲酯（30微摩尔）也以与NOARG相似的效力抑制ACh诱导的血管舒张。L-精氨酸（30 - 150微摩尔）而非D-精氨酸（100微摩尔）使L-NOARG（15微摩尔）和L-NMMA（30微摩尔）的抑制作用产生分级逆转。150微摩尔L-精氨酸可完全逆转两种抑制剂的作用。L-丙氨酸（50微摩尔）、L-精氨琥珀酸（5微摩尔）、L-瓜氨酸（50微摩尔）、L-甲硫氨酸（50微摩尔）和L-鸟氨酸（50微摩尔）未能逆转L-NOARG（15微摩尔）的抑制作用。4. L-NOARG（10 - 200微摩尔）和L-NMMA（30 - 100微摩尔）抑制ACh（0.006 - 18.0纳摩尔）对大鼠肠系膜的血管舒张作用，而不影响NP（1.1 - 11.1纳摩尔）引起的血管舒张。L-精氨酸（100微摩尔）而非D-精氨酸（100微摩尔）使L-NOARG（30微摩尔）和L-NMMA（30微摩尔）的作用产生部分逆转。5. L-和D-N'-丁氧羰基No-硝基精氨酸（100微摩尔）对ACh对兔主动脉的作用产生适度（约20%）抑制；这种作用不能被L-精氨酸（100微摩尔）逆转。L-单苄氧羰基精氨酸（L-NMCA，50微摩尔）、L-N-NG-二苄氧羰基精氨酸（L-NDCA，5微摩尔）和L-NG-甲苯磺酰精氨酸（50微摩尔）无活性。6. 这些结果确定L-NOARG是一种强效的、L-精氨酸可逆的内皮依赖性血管舒张抑制剂。现有数据表明，L-NOARG与L-NMMA一样，抑制内皮一氧化氮（NO）生物合成。

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